The genetics and epigenetics of autoimmune diseases.
The genetics and epigenetics of autoimmune diseases.
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DOI：
10.1016/j.jaut.2009.03.007
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发表时间：
2009-08
影响因子：
12.8
通讯作者：
Richardson B
中科院分区：
文献类型：
--
作者：
Hewagama A;Richardson B
自身耐受性丧失是自身免疫的基础。虽然对免疫调节的理解正在迅速扩大，但在大多数自身免疫性疾病中导致耐受性丧失的机制仍然难以捉摸。据信，当遗传易感个体遇到引发疾病的环境因子时，就会发生自身免疫。遗传和环境因素对自身免疫作用的最新进展表明，遗传因素和环境因素引起的表观遗传变化之间的相互作用可能是诱发自身免疫性疾病的原因。诱发自身免疫的遗传位点正在通过多中心联盟进行鉴定，并且经验证的基因数量正在迅速增长。最近的报告还表明，环境可以通过表观遗传机制修饰基因表达来促进自身免疫。本文以系统性红斑狼疮为例，综述了目前对狼疮、类风湿性关节炎、多发性硬化症和1型糖尿病的遗传学和表观遗传学的认识。其他自身免疫性疾病可能有类似的基础。
Self tolerance loss is fundamental to autoimmunity. While understanding of immune regulation is expanding rapidly, the mechanisms causing loss of tolerance in most autoimmune diseases remain elusive. Autoimmunity is believed to develop when genetically predisposed individuals encounter environmental agents that trigger the disease. Recent advances in the genetic and environmental contributions to autoimmunity suggest that interactions between genetic elements and epigenetic changes caused by environmental agents may be responsible for inducing autoimmune disease. Genetic loci predisposing to autoimmunity are being identified through multi-center consortiums, and the number of validated genes is growing rapidly. Recent reports also indicate that the environment can contribute to autoimmunity by modifying gene expression through epigenetic mechanisms. This article will review current understanding of the genetics and epigenetics of lupus, rheumatoid arthritis, multiple sclerosis and type 1 diabetes, using systemic lupus erythematosus as the primary example. Other autoimmune diseases may have a similar foundation.
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影响因子：
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作者：
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